Causes of atherosclerosisThere are several
theories about how
atherosclerosis occurs. Response-to-injury theory The response-to-injury theory suggests that atherosclerosis
develops as a result of repetitive injury to the inner lining of the artery.
This injury could be caused by any number of factors, including: - Physical stress on the artery lining, such as
stress caused by
high blood pressure.
- A response to an
infection within the artery wall.
- Oxidative damage to the artery
lining. Oxidative damage refers to injury caused by unstable molecules called
free radicals. Free radicals are formed during reactions between oxygen and LDL
("bad" or low-density lipoprotein) cholesterol.
- High cholesterol. Cholesterol is a major part of the
plaque that develops in atherosclerosis. People with elevated LDL ("bad")
cholesterol levels or low HDL ("good" or high-density lipoprotein) cholesterol
levels are known to have increased risk of
coronary artery disease and
stroke. Lowering cholesterol levels through diet,
exercise, and medication clearly reduces these risks, providing strong evidence
of the link between cholesterol and atherosclerosis. Exactly why high
cholesterol levels promote plaque formation is not clear. Cholesterol is found
normally in all cell membranes, but it may alter the physical properties of the
blood vessel wall, making it more susceptible to damage. Oxidized LDL
cholesterol may cause injury to the blood vessel wall and promote an
inflammatory reaction that clogs the artery lining with debris.
Injury may stimulate cells to grow and divide as part of the
inflammatory process. This normal, healing response to chronic injury may
actually result in the growth of atherosclerotic plaque. Growth factors One of the major features of atherosclerosis is the abnormal
growth of smooth muscle cells and immune cells in the plaque. Chemical
messengers called growth factors cause these cells to grow and divide. A better
understanding of the roles of growth factors may eventually lead to treatments
that block the development of atherosclerotic plaque.
| | Author: | Douglas Dana Robin Parks, MS | Last Updated: September 21, 2007 | | Medical Review: | Anne C. Poinier, MD - Internal Medicine Caroline S. Rhoads, MD - Internal Medicine Stephen Fort, MD, MRCP, FRCPC - Interventional Cardiology Robert A. Kloner, MD, PhD - Cardiology Ruth Schneider, MPH, RD - Diet and Nutrition | © 1995-2008 Healthwise, Incorporated. Healthwise, Healthwise for every health decision, and the Healthwise logo are trademarks of Healthwise, Incorporated.This information does not replace the advice of a doctor. Healthwise disclaims any warranty or liability for your use of this information. Your use of this information means that you agree to the Terms of Use. How this information was developed to help you make better health decisions.
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